In July this year a group of researchers published a paper (open access) in Pain asking if we need a third mechanistic descriptor for chronic pain states. It was an interesting read, and here are some of their main points …
A bit of history
Currently the IASP taxonomy provides two classifications of pain states:
Neuropathic pain – pain caused by a lesion or disease of the somatosensory nervous system
Nociceptive pain – pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.
This definition of neuropathic pain is relatively new, amended in 2011. The previous 19994 definition included ‘pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation of the peripheral or central nervous system’. Notably, the word dysfunction has been removed and the system is now referred to as the somatosensory nervous system. It was thought that the previous definition was limited in its ability to distinguish neuropathic pain conditions in a clinically meaningful way.
‘The clinical challenge is to identify and ameliorate the cause(s) of the pain, which may be tissue damage, damage to the body’s warning system, both, or neither. We are not doing the patients any good by giving them a diagnostic label for which there is no basis.’
So what’s the problem?
Not everyone is happy. This new definition has left a large group of patients without a valid pathophysiological descriptor for their experience of pain.
Not only does it miss those with lesions in areas outside the somatosensory nervous system (i.e. the cerebellum or frontal cortices) but notably it also misses those whose pain is not due to neuropathy but for whom activation of nociceptors also cannot be confidently established – i.e. fibromyalgia, musculoskeletal pain (such as non-specific back pain) and visceral pain disorders (such as irritable bowel syndrome, bladder pain syndrome).
What to do with the gap
This gap has led to the pain of some groups being termed ‘idiopathic’ or ‘pain of unknown origin’, and some are calling to reinstate the 1994 definition, saying that this new definition of neuropathic pain is too restrictive and has the potential to suffocate new research. However, others don’t agree. They are happy to accept the new definition, but believe it warrants a third category to fill this caveat.
Some interesting suggestions come from a 2016 paper by Kosek et al.
‘It is proposed that a new term be introduced to describe pain states characterised by clinical and psychophysical findings that suggest altered nociception, despite there being no clear evidence of actual or threatened tissue damage causing the activation of nociceptors or evidence for disease or lesion of the somatosensory system causing the chronic pain.’
So here are their suggestions:
Nociplastic: arising from ‘nociceptive plasticity’ to reflect change in function of nociceptive pathways.
Algopathic: which combines ‘algos’ (Greek for pain) with ‘pathic’ (Greek for suffering) to reflect a pathological sensation of pain not generated by injury.
Nocipathic: from ‘nociceptive pathology’ to reflect a pathological (ie. not “normal”) state of nociception.
Note: The terms are intended for clinical usage and are neither a diagnosis nor a synonym for ‘central sensitisation of nociception,’ which is a neurophysiological concept.
So do we need a third descriptor? Although these pain conditions have unexplained mechanisms, should we still provide them a mechanistic category more defind then ‘idiopathic‘? And if so, do any of these suggestions float your boat?
– Hayley Leake
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